Coccidioidomycosis is caused by infection with Coccidioides immitis or Coccidioides posadasii (collectively “Coccidioides”). C. immitis and C. posadasii are the fungal etiologic agents of coccidioidomycosis (Valley Fever) and are endemic to arid soils of the southwest United States, as well as parts of Mexico, and Central and South America. Primary hosts acquire Coccidioides via inhalation of aerosolized arthroconidia upon soil disruption. Coccidioidomycosis most commonly causes a progressive pulmonary infection in humans and other vertebrate hosts but also can disseminate to other body parts including the skin, brain, bone, and meninges. This disseminated secondary coccidioidomycosis often is severe and can result in patient death. However, in cases where infection is resolved, patients usually acquire a specific and lifelong immunity to the fungus.
Coccidioidomycosis infection rates have increased dramatically in the last decade with the State of Arizona documenting the number of reported cases per 100,000 people having increased from 20.8 in 1997 to 186.0 in 2010. Increased physician awareness and testing likely accounts for a portion of this case increase. An additional cause for this increase may be influxes of immunologically naive individuals into Arizona. A significant number of individuals from outside the Coccidioides endemic region migrate annually to the desert southwest and are at greater risk for developing coccidioidomycosis, even after returning to their respective homes. These infections, therefore, are likely to escape or confound diagnosis in non-endemic regions.
For individuals with Valley Fever, there are limited treatment options and scant options in drug-discovery pipelines. Moreover, the extreme costs associated with developing and receiving FDA approval for a new chemical entity for the treatment of Valley Fever is a significant deterrent for most businesses. As such, there is an ongoing need to develop treatments for Valley Fever that comprise known compounds.